OBJECTIVE: Ventilator-induced lung injury is a risk in patients requiring elevated ventilatory support pressures. We hypothesized that thermal stress modulates the development of ventilator-induced lung injury. DESIGN: Experimental study. SETTING: University laboratory. SUBJECTS: Anesthetized rabbits. INTERVENTIONS: Two experimental studies were designed to determine the role of temperature as a cofactor in ventilator-induced lung injury. In the first study, three groups of anesthetized rabbits were randomized to be ventilated for 2 hrs at core body temperatures of 33, 37, or 41 degrees C while ventilated with pressure control ventilation of 15/3 cm H2O (noninjurious settings-control) or 35/3 cm H2O (potentially injurious settings-experimental). To exclude effects arising from cardiac output fluctuations or from extrapulmonary organs, an isolated lung model was used for the second study, perfused at a fixed rate and studied at either 33 degrees C or 41 degrees C. MEASUREMENTS AND MAIN RESULTS: In the first study, the hyperthermic group compared with the hypothermic animals had significantly reduced mean PaO2 (-114 vs. + 14 mm Hg, p <.05), increased lung edema formation (mean wet weight/dry weight ratio of 8.1 vs. 5.7), and altered pressure-volume curves. The hyperthermic isolated, perfused lungs had an increased ultrafiltration coefficient, formed more edema, and experienced greater alveolar hemorrhage than hypothermic lungs. CONCLUSIONS: In two studies of ventilator-induced lung injury in rabbits, maintaining hyperthermia compared with hypothermia augmented the development of lung injury. Similar results from both the in vivo and isolated, perfused lung studies suggest that the observed effects were not due to cardiovascular factors or consequences of heating nonpulmonary organs.
OBJECTIVE: Ventilator-induced lung injury is a risk in patients requiring elevated ventilatory support pressures. We hypothesized that thermal stress modulates the development of ventilator-induced lung injury. DESIGN: Experimental study. SETTING: University laboratory. SUBJECTS: Anesthetized rabbits. INTERVENTIONS: Two experimental studies were designed to determine the role of temperature as a cofactor in ventilator-induced lung injury. In the first study, three groups of anesthetized rabbits were randomized to be ventilated for 2 hrs at core body temperatures of 33, 37, or 41 degrees C while ventilated with pressure control ventilation of 15/3 cm H2O (noninjurious settings-control) or 35/3 cm H2O (potentially injurious settings-experimental). To exclude effects arising from cardiac output fluctuations or from extrapulmonary organs, an isolated lung model was used for the second study, perfused at a fixed rate and studied at either 33 degrees C or 41 degrees C. MEASUREMENTS AND MAIN RESULTS: In the first study, the hyperthermic group compared with the hypothermic animals had significantly reduced mean PaO2 (-114 vs. + 14 mm Hg, p <.05), increased lung edema formation (mean wet weight/dry weight ratio of 8.1 vs. 5.7), and altered pressure-volume curves. The hyperthermic isolated, perfused lungs had an increased ultrafiltration coefficient, formed more edema, and experienced greater alveolar hemorrhage than hypothermic lungs. CONCLUSIONS: In two studies of ventilator-induced lung injury in rabbits, maintaining hyperthermia compared with hypothermia augmented the development of lung injury. Similar results from both the in vivo and isolated, perfused lung studies suggest that the observed effects were not due to cardiovascular factors or consequences of heating nonpulmonary organs.
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